Oxidative stress (OS) arises when the body is subjected to harmful endogenous or exogenous factors that overwhelm the antioxidant system. There is increasing evidence that OS is involved in a number of diseases, including ovarian cancer (OC). OC is the most lethal gynecological malignancy, and risk factors include genetic factors, age, infertility, nulliparity, microbial infections, obesity, smoking, etc. OS can promote the proliferation, metastasis, and therapy resistance of OC, while high levels of OS have cytotoxic effects and induce apoptosis in OC cells. This review focuses on the relationship between OS and the development of OC from four aspects: genetic alterations, signaling pathways, transcription factors, and the tumor microenvironment. Furthermore, strategies to target aberrant OS in OC are summarized and discussed, with a view to providing new ideas for clinical treatment.

Sleep disorders, such as insomnia, sleep terrors, sleep apnea, and sleep-wake schedule disorders, pose a significant public health challenge worldwide, yet their underlying pathophysiological mechanisms are not fully understood. Lipids, beyond being structural membrane components, actively regulate neuroinflammation, circadian rhythms, and neuronal signaling, all implicated in sleep disorder pathophysiology. This study employed two-sample Mendelian randomization (TSMR) to explore the causal relationships between the lipidome and these sleep disorders, analyzing a comprehensive GWAS dataset with 179 lipid species. Heterogeneity and pleiotropy were assessed using Cochran Q test, MR-Egger intercept test, and MR-PRESSO global test, and sensitivity analyses were done to check the influence of individual single nucleotide polymorphisms. The analysis revealed significant causal associations between specific lipid species and sleep disorders. For insomnia, several lipid species, including sterol ester (27:1/20:3), ceramides (d40:1, d42:1, d42:2), phosphatidylcholine (15:0_18:2), and sphingomyelin (d40:1), demonstrated potential protective effects (OR < 1). In contrast, for sleep terrors, phosphatidylcholines (16:0_22:4, O–16:0_16:1, O–16:0_18:2) and sphingomyelin (d34:0) were associated with increased risk (OR > 1), while triacylglycerol (46:2) showed a protective effect. For sleep apnea, cholesterol levels exhibited a protective effect (OR = 0.96), whereas specific phosphatidylcholines (16:1_18:0) and triacylglycerols (52:2, 52:3, 58:8) were associated with increased risk. Circadian rhythm disturbances were influenced by various lipid species, with diacylglycerol (18:1_18:3) and phosphatidylcholine (16:1_18:0) posing risk-increasing effects, while phosphatidylethanolamines (O–16:1_20:4, O–18:1_20:4) demonstrated protective roles. This study elucidates the complex interplay between lipid metabolism and sleep regulation, identifying specific lipid species that may serve as potential biomarkers or therapeutic targets for sleep disorders.

Lactic acid modification of histones represents an emerging post-translational modification that establishes a critical link between cellular metabolic reprogramming and epigenetic regulation through the covalent binding of lactic acid to histone lysine residues. In recent years, the mechanisms underlying this modification in the pathogenesis of various diseases have been progressively elucidated, revealing its extensive biological impact and potential clinical translational value. As research progresses, the functional role of histone lactylation in gynecological diseases has become increasingly evident, offering a novel epigenetic perspective for deciphering the pathogenesis of gynecological-related disorders. This review outlines the mechanisms underlying histone lactylation and focuses on its regulatory role in common benign and malignant gynecological diseases. The malignant diseases discussed include ovarian, endometrial, and cervical cancers, while the benign conditions include endometriosis and polycystic ovary syndrome. Furthermore, it undertakes an analysis of the therapeutic potential of histone lactylation modifications and reviews emerging targeted therapeutic strategies. These include targeting lactate production, lactate transport, lactylation-associated enzymes, or downstream effectors, highlighting their potential to intervene in disease progression. The present study aims to systematically elucidate the core value of histone lactylation as a novel epigenetic link between metabolism and gynecological disease pathogenesis. In addition, it provides clear research directions and robust theoretical support for developing targeted therapeutic strategies based on lactylation modifications.